Guillermo Gutierrez

Clinical review: Hemorrhagic shock

This review addresses the pathophysiology and treatment of hemorrhagic shock – a condition produced by rapid and significant loss of intravascular volume, which may lead sequentially to hemodynamic instability, decreases in oxygen delivery, decreased tissue perfusion, cellular hypoxia, organ damage, and death. Hemorrhagic shock can be rapidly fatal. The primary goals are to stop the bleeding and to restore circulating blood volume. Resuscitation may well depend on the estimated severity of hemorrhage. It now appears that patients with moderate hypotension from bleeding may benefit by delaying massive fluid resuscitation until they reach a definitive care facility. On the other hand, the use of intravenous fluids, crystalloids or colloids, and blood products can be life saving in those patients who are in severe hemorrhagic shock. The optimal method of resuscitation has not been clearly established. A hemoglobin level of 7–8 g/dl appears to be an appropriate threshold for transfusion in critically ill patients with no evidence of tissue hypoxia. However, maintaining a higher hemoglobin level of 10 g/dl is a reasonable goal in actively bleeding patients, the elderly, or individuals who are at risk for myocardial infarction. Moreover, hemoglobin concentration should not be the only therapeutic guide in actively bleeding patients. Instead, therapy should be aimed at restoring intravascular volume and adequate hemodynamic parameters.

Central venous to mixed venous blood oxygen and lactate gradients are associated with outcome in critically ill patients

ObjectiveBlood O2 saturation and lactate concentration gradients from superior vena cava (SVC) to pulmonary artery (PA) occur in critically ill patients. These gradients (ΔSO2 and Δ[Lac]) may be positive or negative. We tested the hypothesis that positive ΔSO2 and Δ[Lac] are associated with improved survival in critically ill patients.Design and settingMultinational, prospective observational study conducted in six medical and surgical ICUs.PatientsConsecutive sample of 106 adults requiring insertion of a pulmonary artery catheter (PAC). Average age was 59.5xa0±xa015.5xa0years, APACHE II score was 15.5xa0±xa06.7 (meanxa0±xa0SD). Main outcome measure was 28-day mortality.InterventionsNone.Measurements and resultsWe drew blood samples from the proximal and distal ports of PACs every 6xa0h from the time of PAC insertion (Initial measurement) until its removal (Final measurement). Samples were analyzed for SO2, [Lac], glucose concentration and blood gases. Hemodynamic measurements were obtained after blood samples. We monitored patients for 30.9xa0±xa011.0xa0h. Overall mortality rate was 25.5%. More survivors had mean and final ΔSO2xa0≥xa00 and Δ[Lac]xa0≥xa00 than decedents (pxa0<xa00.01; pxa0<xa00.05 respectively). On the average, ΔSO2 and Δ[Lac] were positive in survivors and negative in decedents. Survival odds ratios for final measurements of ΔSO2xa0≥xa00 and Δ[Lac]xa0≥xa00 were 19.22 and 7.70, respectively (pxa0<xa00.05).ConclusionsA strong association exists between positive ΔSO2 and Δ[Lac] and survival in critically ill patients. Whether therapy aimed at increasing ΔSO2 and Δ[Lac] results in improved ICU survival remains to be determined.

Blood flow, not hypoxia, determines intramucosal PCO2

Monitoring tissue hypoxia in critically ill patients is a challenging task. Tissue PCO2 has long been proposed as a marker of tissue hypoxia, although there is considerable controversy on whether the rise in CO2 with hypoxia is caused by anaerobic metabolism and excess CO2 production or by the accumulation of aerobically produced CO2 in the setting of blood flow stagnation. The prevention of increases in intestinal PCO2 in aggressively resuscitated septic animals supports the notion that tissue CO2 accumulation is a function of decreases in blood flow, not of tissue hypoxia.

The concentration of oxygen, lactate and glucose in the central veins, right heart, and pulmonary artery: a study in patients with pulmonary hypertension

IntroductionDecreases in oxygen saturation (SO2) and lactate concentration [Lac] from superior vena cava (SVC) to pulmonary artery have been reported. These gradients (ΔSO2 and Δ[Lac]) are probably created by diluting SVC blood with blood of lower SO2 and [Lac]. We tested the hypothesis that ΔSO2 and Δ[Lac] result from mixing SVC and inferior vena cava (IVC) blood streams.MethodsThis was a prospective, sequential, observational study of hemodynamically stable individuals with pulmonary artery hypertension (n = 9) who were about to undergo right heart catheterization. Catheters were advanced under fluoroscopic guidance into the IVC, SVC, right atrium, right ventricle, and pulmonary artery. Samples were obtained at each site and analyzed for SO2, [Lac], and glucose concentration ([Glu]). Analysis of variance with Tukey HSD test was used to compare metabolite concentrations at each site.ResultsThere were no differences in SO2 or [Lac] between IVC and SVC, both being greater than their respective pulmonary artery measurements (P < 0.01 for SO2 and P < 0.05 for [Lac]). SO2 and [Lac] in right atrium, right ventricle, and pulmonary artery were similar. ΔSO2 was 4.4 ± 1.4% (mean ± standard deviation) and Δ[Lac] was 0.16 ± 0.11 mmol/l (both > 0; P < 0.001). Δ[Glu] was -0.19 ± 0.31 mmol/l, which was not significantly different from zero, with SVC [Glu] being less than IVC [Glu].ConclusionMixing of SVC with IVC blood does not account for the development of ΔSO2 and Δ[Lac] in hemodynamically stable individuals with pulmonary artery hypertension. An alternate mechanism is mixing with coronary sinus blood, implying that ΔSO2 and Δ[Lac] may reflect changes in coronary sinus SO2 and [Lac] in this patient population.

Lactate concentration gradient from right atrium to pulmonary artery.

IntroductionWe compared simultaneous measurements of blood lactate concentration ([Lac]) in the right atrium (RA) and in the pulmonary artery (PA). Our aim was to determine if the mixing of right atrial with coronary venous blood, having substantially lower [Lac], results in detectable decreases in [Lac] from the RA to the PA.MethodsA prospective, sequential, observational study was conducted in a medical-surgical intensive care unit. We enrolled 45 critically ill adult individuals of either sex requiring pulmonary artery catheters (PACs) to guide fluid therapy. Immediately following the insertion of the PAC, one paired set of blood samples per patient was drawn in random order from the PACs proximal and distal ports for measurement of hemoglobin concentration, O2 saturation (SO2) and [Lac]. We defined Δ[Lac] as ([Lac]ra - [Lac]pa), ΔSO2 as (SraO2 - SpaO2) and the change in O2 consumption (ΔVO2) as the difference in systemic VO2 calculated using Ficks equation with either SraO2 or SpaO2 in place of mixed venous SO2. Data were compared by paired Students t-test, Spearmans correlation analysis and by the method of Bland and Altman.ResultsWe found SraO2 > SpaO2 (74.2 ± 9.1 versus 69.0 ± 10.4%; p < 0.001) and [Lac]ra > [Lac]pa (3.9 ± 3.0 versus 3.7 ± 3.0 mmol.l-1; p < 0.001). Δ[Lac] correlated with ΔVO2 (r2 = 0.34; p < 0.001).ConclusionWe found decreases in [Lac] from the RA to PA in this sample of critically ill individuals. We conclude that parallel decreases in SO2 and [Lac] from the RA to PA support the hypothesis that these gradients are produced by mixing RA with coronary venous blood of lower SO2 and [Lac]. The present study is a preliminary observation of this phenomenon and further work is needed to define the physiological and clinical significance of Δ[Lac].

Of hemorrhagic shock, spherical cows and Aloe vera

The central question explored in this commentary is whether the beneficial effects of an Aloe vera derived drag-reducing polymer during hemorrhagic shock is due to its O2 radical scavenging properties or to changes in blood rheology.

Baum's Textbook of Pulmonary Diseases, 7th Edition.

Many years ago, longer than I may care to admit, I had to take my Board Exam in Pulmonary Medicine. I decided to prepare for the exam by reading a reference textbook cover-to-cover. Since Dr. Gerald Baum had been one of my favorite teachers while a medical student in Cleveland, I naturally felt inclined towards an earlier edition of Baums Textbook of Pulmonary Medicine. It was a most fortunate decision, since not only did I pass the Board Exam, but I much enjoyed the concise yet comprehensive style of the textbook that help me fill several lacunae of knowledge left over from my years in training.